Ultraviolet light-induced tumors were selected for various host-tumor relationships and adapted to tissue culture, so the mechanism of tumor regression could be compared to the reactivity, or lack of it, induced by progressor UVL-induced tumors. Regressor-injected recipients developed a specific immune response which was measurable in vitro, directed by T lymphocytes and resulted in tumor rejection. Regression could be correlated with specific immune reactivity measured in vitro from both systemic and in situ comparments. Transplantation studies showed that progressor tumors contained tumor specific transplantation antigens (TSTA) even though they grew progressively. Progression could be correlated with a lack of specific immune reactivity tested both systemically and in situ. An analysis of the types of lymphoid cells within the subcutaneous tumor site showed 10-fold more T lymphocytes in the regressing tumors than in the progressing tumors, few B lymphocytes in either group, and a substantial number of non-T, nonB lymphocytes. Experiments were performed to determine if effector cell induction was blocked. Splenic lymphocytes from tumor-bearing hosts cultured in vitro without antigen and tested for immune reactivity against the homologus tumor cells showed high cytotoxic reactivity. Mice treated intraperitoneally with cyclophosphamide before subcutaneous injection of progressor tumor cells showed no tumor growth. Thus, UVL-induced progressor tumors grow because the immune reactivity is suppressed and not because they have no TSTA to induce a response.